INTERVIEWER Marc Hellerstein thought that the obesity epidemic was caused by people being sedentary?

TAUBES He believed that the key is whether you’re sedentary compared to how you used to be. When I told him about the Pima and the Sioux Indians and this 1981 study of obesity in oil field workers, he had an excuse for everything. So the Pima and the Sioux Indians, they lived on reservations, so they could be obese because they were relatively sedentary, at least more sedentary than they used to be. And the oil field workers, well, they’re Mexican-American, so they have some kind of “thrifty” gene going. You know…this is what pathological science is: a field in which you can find a reason to explain away all negative evidence. In pathological science, it’s no longer possible to refute the hypothesis. Remember, science is about trying to test your hypothesis and refute it, but in a field like this, if you test it and come up with a counter-example, the counter-example is just explained away with whatever comes to mind. Negative evidence never means anything. So you have an obese person who’s sedentary, that’s proof of my hypothesis. If you have an obese person who’s very active — at least, compared to most people today — the Sioux indians, for instance, who were so poor they had to walk down to the river to get their drinking water; who had no televisions, no cars; they had to walk outside to evacuate their bowels — those people are obese because they used to be more active than they are now.

INTERVIEWER I’ve never heard that before: “They used to be more active.”

TAUBES But that’s the implication of Hellerstein’s knee-jerk reservation hypothesis. They may be poor, and they may be out working in the fields, so compared to us, they’re active, but compared to their former life, they’re sedentary. See what I’m saying?

INTERVIEWER Yeah, I understand the logic. I’ve just never heard it before.

TAUBES Well, the reason you’ve never heard it before is because you’ve never heard anyone have to explain why obesity was common in an impoverished Native American tribe in 1902 or in 1928. When confronted with that observation, they have to come up with an explanation so that they don’t have to question their hypothesis. I happen to challenge someone who believes the conventional wisdom unconditionally, and that’s the response I get: “Well, they’re living on reservations”.

INTERVIEWER Does he do research on weight, on obesity?

TAUBES Absolutely, he does.

INTERVIEWER That’s unfortunate.

TAUBES This is why the field is in the position it’s in. These people believe so strongly in the calories in/calories out/gluttony/sloth combination that they no longer function as scientists. They can’t imagine the existence of an alternative hypothesis. So everything they see, they have to find a way to interpret it so that it supports what they already believe to be true.

INTERVIEWER They don’t see that they’re operating differently…

TAUBES …than other scientists.

INTERVIEWER Do they see that they’re not making progress?

TAUBES No, because that gets blamed on the obese. If you believe that obesity is caused by sloth, then the reason fat people are fat is because they don’t have the moral fortitude to go run ten miles every day the way you do.

INTERVIEWER Well, people have been saying that for 50 or 60 years. So the fact that they’re saying the same thing now as they were saying 60 years is a sign, to me, that they’re not making progress.

TAUBES Yes, that’s a very good sign, but these people don’t realize they’re saying the same things and doing the same experiments and making the same mistakes that their predecessors made a century go because they don’t bother reading that literature. For reasons I still don’t really understand, these people see no reason to pay attention to the history of their field. Imagine if physicists saw no reason to pay attention to Einstein and Plank and Maxwell and Heisenberg? I mean, these guys all lived a century ago, why would anyone want to know about them or the experiments they did? But in physics, mathematics and even biology, the history is carried along with it. As the science progresses, it takes with it the successful ideas and the students learn about the history along with the science. In obesity research, World War II just cut all of that off. For whatever reason, several generations of researchers grew up with this belief that the history of the field doesn’t matter. And so they don’t even know or care that they’re saying the same thing and doing the same experiments that their predecessors did 100 years ago. And then this latest generation is full of young molecular biologists, and they start the clock in 1994, when leptin was discovered. They’re not aware that they’re not making progress, because they believe that nothing of value was done until 1994.

INTERVIEWER The birth of a new world. In your book, you seem to place weight on the fact that Atkins was disliked by people he went to school with. Did I read that wrong?

TAUBES I think that was part of it. I think the fundamental problem with Atkins is that his book emerged in 1972 , when the low-fat dogma was really beginning to be taken seriously, not just by the heart disease researchers, but by physicians and public health authorities. It was viewed as a great triumph of modern medicine. We finally understand what causes heart disease. Then Atkins goes out of his way to throw the high-fat nature of his diet out there: “You can eat Lobster Newberg, double cheeseburgers, and porterhouse steaks” (like my New York Times Magazine cover). The AMA always had this philosophy that even if people wanted to lose weight, they should go to their doctor and discuss it with them. You shouldn’t go on a diet without your physician’s guidance. So here Atkins was end-running all of that. Then he was saying “eat a high-fat diet. It’s harmless”. He actually said “It’s good for you.” If you read Atkins, he read a lot of the papers I read. His understanding wasn’t tremendously sophisticated, but he didn’t have the advantage I had, of coming along 40 years later. For the time, he was doing pretty damned good. He believed that triglycerides were the problem, not cholesterol. He believed that insulin was a problem. He was a working physician; he didn’t have the time that I did to read all of the research, and to have the internet available to allow him to track down all of the references. But the establishment thought his diet was dangerous. And then Atkins made these claims that he had patients who consumed 5000 calories a day and still lost weight, so they also believed Atkins was a quack, a shyster trying to sell impossible dreams. And they thought this because they believed that calories in/calories out was all that mattered. They had this inherent belief that in order to lose weight, you have to restrict calories; Atkins said you didn’t. So, to these establishment nutrition types, Atkins was saying that the laws of thermodynamics can be ignored. So they had reason to think that Atkins’s diet couldn’t possibly work, on the one hand, and that it would kill you, on the other. So these “responsible physicians,” as they perceived themselves to be, felt an obligation to suppress this threat to the public health. The fact that they knew Atkins personally, that some of them had worked with him and gone to medical school with him and didn’t particularly like him, made it all that much more . . .

INTERVIEWER Irresistible.

TAUBES Yes, irresistible. One of the things I mentioned in my lecture was something I didn’t realize this when I wrote the book. Atkins proposed that one reason carbohydrates-restriction worked is that it stimulated the secretion of something that British researchers in the 1950s had called Fat Mobilizing Hormone. The joke is that you didn’t need a Fat Mobilizing Hormone; the thing you have to do to mobilize fat is lower insulin levels and the way to do that is to remove the carbohydrates from the diet. That’s what mobilizes fat from the fat tissue. But Atkins was doing what a lot of diet book authors do, which was combing the literature for everything and maybe anything that might support his argument. He talked about insulin, but he also talked a lot about Fat Mobilizing Hormone, which was controversial at the time but not an outrageous idea. At the time Atkins wrote the book, this Fat Mobilizing Hormone had yet to be nailed down, and it never would be. The fundamental requirement to mobilize fat, as I said, is to lower insulin. So, the American Medical Association publishes this famous article dedicated, effectively, to establishing that Atkins has no credibility and one of the ways they do it is to discuss how Atkins was wrong about this idea of Fat Mobilizing Hormone. Then in the same paragraph they also say “in order to mobilize fat, you have to lower insulin”. Then they go back to talking about how Atkins jumped the gun on Fat Mobilizing Hormone . So they know that insulin controls fat accumulation, and they say actually acknowledge it in the article, but only in the context of it supporting the argument that Atkins has no credibility. They never mention that the way to lower insulin — and so, apparently, to mobilize fat from the fat tissue — is to eat less carbohydrates, which is exactly what Atkins was recommending. I was writing my response to Gina Kolata’s review when I first really noticed that sentence, and it jumped out at me. “Holy shit!” These people knew what regulates fat tissue, and they know what regulates insulin. They just don’t care. That’s how dedicated they were to trying to squash Atkins.

INTERVIEWER It didn’t matter whether evidence supported them or that there was something there that they couldn’t explain. It just mattered that he was wrong about something.

TAUBES All they wanted to do was establish that Atkins was not a credible source, and people shouldn’t follow these bizarre practices of nutrition, or whatever they called it. One of the things I’m curious about is whether, from here on, the American Heart Association and other health authorities will continue to refer to low-carb diets, the Atkins diet, as these fad diets. Even though, if nothing else, as I point out in the book, these diets constituted the preferred medical treatment of obesity for 150 years, or 100 years, until the low-fat diet came along. It’s the low-fat diet that’s the fad.

INTERVIEWER That’s an interesting point. What is the fad diet? Is it the absence of the Atkins Diet, or its presence? Which is temporary?

TAUBES The idea that you could somehow lose weight by removing fat and increasing carbohydrates is as ludicrous as the idea that you could do it by eating ice cream for any extended period of time. I’m sure there’s something about the ice cream diet that works in the short term. I’m not sure, but I wouldn’t be surprised.

INTERVIEWER Was your response to Kolata’s review published?

TAUBES Yes. If you search me in the Times, you can read my response.

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INTERVIEWER I was a member of the Center for Weight and Health. But the other members didn’t know what I was up to, and had no idea it could have anything to do with actual weight loss.

TAUBES That’s one of the things I’ve found most amusing about obesity research, that you have this disconnect from pre-World War Two, when the people doing it were clinicians who were treating obese patients, to post-World War Two, where first, it’s nutritionists, who do rat experiments. Then, by the 1960s, obesity is considered an eating disorder and it’s being treated by psychologists and psychiatrists. So today, if you looking at some of the major obesity centers in the country — at Yale, at University of Cincinnati, they’re all run by psychologists or psychiatrists. Here’s a physiological disorder of the body, and it’s being studied by psychologists and psychiatrists. They’re not interested in anecdotal evidence, unless it agrees with their preconceptions.

INTERVIEWER In my department, we don’t have any of that. Obesity is not handled much on the Berkeley campus.

TAUBES But think about it: it’s a physiological disorder.

INTERVIEWER Well, hunger is controlled by the brain.

TAUBES I know, I know, but you know, diabetics get hungry. Type I diabetics are starving. Literally starving, without insulin. But it’s not psychologists who treat diabetics.

INTERVIEWER I think that with Type I diabetes, you can say, “look at this problem; it’s not in the brain”. But I think with most obesity, it’s no so obvious that the problem isn’t in the brain. Sure, they’re fat, but maybe they’re fat because they’re hungry too much. That could easily be a brain disorder. It could easily have something to do with the brain.

TAUBES It could have something to do with the brain, but the problem is in the body. This is the paradigm problem. If you just think of it as hunger, then…

INTERVIEWER I’m not saying you just think of it as hunger, but you wouldn’t want to rule it out.

TAUBES Yeah, I know. That’s why the book is so long, because I’m trying to do it — I’m trying to say “Look, your fat tissue is trying to get fat. Hunger and gluttony and sloth are side-effects of what’s happening at a hormonal level in your fat tissue.”

INTERVIEWER Right. What effect did Weston Price have on you?

TAUBES Price was interesting. It’s funny. He got cut from the book for reasons of length and narrative, but reading Price was a revelation to me, as I say in the acknowledgments. I think that Price should be required reading for every nutritionist in the world. And then, “Nutrition and Physical Degeneration” is a great read, as well.

INTERVIEWER How did you come to read his book?

TAUBES How did I come to Price? I don’t remember, actually. Somebody in the field must have recommended him.

INTERVIEWER It was after your New York Times article?

TAUBES Oh, yes, definitely. I did not read Weston Price prior to that. I have to say, by the way, that I was trying to decide how much to believe of Price’s stories. I decided that if his story about migrating, tree-climbing crabs in the South Pacific was true, I would believe everything Price said. This was my calibration. Because some of his stories are wild: about how pygmies, for instance, kill elephants by slowly hamstringing them over the course of a few days. Even with his photos as evidence, they’re still hard to believe. So, anyway, this being the 21st century, I googled the tree-climbing crabs , and indeed, there are migrating, tree-climbing crabs in the South Pacific. The article I found didn’t say whether the local natives hunted them by putting nets under the trees and making the sounds of coconuts falling, so that the crabs would climb back down into their nets, which is what Price wrote, but the crabs definitely exist. I decided that’s it. As far as I’m concerned, Weston Price is an unimpeachable source.

INTERVIEWER That’s good to know. I really like his work, too.

TAUBES And those photos of the teeth of populations that do and do not eat sugar and white flour. Compelling stuff. I have a 2 year old and I try to keep him away from sugar and white flour just because of Price’s photos. And you know, in this day and age, it’s not easy to keep a child away from sugar and white flour. But it’s the photos in Price’s book that keeps me motivated: we’ve got to survive in Manhattan on a science writer’s salary. It would be nice to save the $6,000 for braces, if I could keep him off sugar and white flour. I still don’t understand how the sugar and flour can effect how the teeth actually grow in, but Price makes a compelling argument that they do.

INTERVIEWER There’s disagreement about that. Weston Price thinks it’s one thing. A professor in Illinois thinks it’s that that people who eat the urban diets have soft food, and the people who eat the rural diets have chewy food. The chewy food makes the kids’ jaws grow to be the right size.

TAUBES My problem with that is that he’s making the assumption that the addition of sugar and flour removes some significant portion of the baseline diet. It could be true, but again, it’s an extra assumption. Take the Inuits, for example: one of the things I did in the course of my research was try to refute this notion that cancer didn’t exist in the Inuits until the 1930s. So I tracked down whatever memoirs I could find from physicians working with the Inuits to see if any of them mentioned cancer prior to the 1930s. And one of the things I found fascinating was that at the turn of the early years of the 20th century, the Inuit were eating mostly their native diet. By the 1950s, they were eating tons of sugar and flour and drinking beer and other alcohol, and tuberculosis had decimated them, but they were still eating their baseline diet; it’s just that all these other things had been added on top. So they’re still eating seal and whale and caribou, but they’re also eating these Western foods. In general, it’s never a good idea to add that extra assumption until you absolutely have to — that something else critical changes with the addition of sugar and flour. Maybe it’s just the addition that’s the cause. That’s the one thing you know for sure that happened. This is Occam’s Razor. The key thing is that cavities are caused by the sugar and flour. The simplest hypothesis is that the orthodontal problems are too. It is possible that the sugar and flour affect growth hormones — insulin-like growth hormone, for instance — which could have local effects on how the teeth grow in. The sugar and flour could affect bacterial growth locally and that could have some effect. Either way, I find the evidence sufficiently compelling to wonder whether my son will grow up with nice teeth if he doesn’t eat a lot of sugar and candy and white flour.

INTERVIEWER Changing the subject slightly, you mentioned that the obesity center at Yale is run by psychologists. Did you ever ask Kelly Brownell how he reconciles his toxic environment view with the fact that many people in poor countries are fat?

TAUBES Not yet. I would like to lecture at Yale some day, and I’m hoping that I don’t have to invite myself. You know, I’m fairly confident that if I were to ask many of these people if they’d get me a lecture — call them and say I’d like to come and talk — they’d arrange it. They ‘re intellectually honest enough on that level. But again, it’s people like Kelly Brownell that I was thinking of when I was compiling that list of populations. And what boggles my mind is that people have been peddling this nonsense for 30 years, and they never bothered to look. They never bothered to do their research, to see if there was evidence that refuted their hypotheses. Again, this is what you do in science; you get a hypothesis, and you try to test it. So how would you test the hypothesis that prosperity causes obesity, or that our modern toxic environment, as defined by Brownell, is the cause. Let’s see if we can find examples of non-toxic populations, you know, poor populations without McDonald’s, without televisions, without remote controls, who are obviously physically active, at least by our standards. It’s funny, I was talking with Hellerstein at Berkeley. When I told him about the Pima and the Sioux Indians, and he said “Well, do they live on reservations?” Like, if they live on reservations, then that means they’re sedentary, at least relatively, compared to their previous lives, and so you can evoke sedentary behavior as the cause of their obesity. So now you have this idea that it’s not how sedentary you are, it’s how sedentary you are in comparison to how active you used to be. So like, Sioux Indians, who rode along the Great Plains and chased after Custer — they were so active that if they only have to move onto reservations and stop riding their horses all the time, they get obese. So it can actually be a detriment to be extremely active, because then being only mildly active causes obesity.

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INTERVIEWER When I started your book, I already kind of believed all of your main points. Not all of them, but I was sympathetic. I knew where it was going. I thought “Oh, good. More evidence. This is interesting, and that’s an interesting way to tell that story”.

TAUBES The way I see it is that the establishment has an immune system to protect itself from challenges. Every science needs that kind of immune system to protect itself from quacks and easy-to-swallow but erroneous ideas that might infect the good science in the field. My question is whether I can infect enough people, enough serious scientists, that I can pose a threat to this immune system, that I could compromise the immune system of the establishment and make them take this idea seriously. Because some times these immune systems work against challenges that are legitimate. I honestly don’t know if I can. It’s going to be an interesting year. I hope I don’t become one of those bitter old men who, when I fail to do so, who can’t let it go.

INTERVIEWER How did you end up giving your recent talk at Berkeley? Obviously someone in the establishment was willing to invite you?

TAUBES Yes. It was actually epidemiologists at the School of Public Health who invited me initially to talk about epidemiology after I had a cover story called “Unhealthy Science” in the New York Times. I told them that the subtext of that story was my book. If what I say in the book is correct, then an observational epidemiology has done an enormous amount of damage. One line that was taken out of the New York Times article said that this was a story about the risks and benefits of observational epidemiology. There are certainly some successes in that endeavor, but if we’re living through an obesity and diabetes epidemic because of its failures, then it’s conceivable that more people have died because of observational epidemiology than have been saved. You always have to look at the negatives, the false negatives and the false positives. You can’t just look at the true positives and say that this is a valuable field of science. We’re digressing again, but the game of poker is relevant here. Are you a poker player?

INTERVIEWER I’ve played a lot of poker, yeah.

TAUBES Bad poker players base their methodology, their strategy, only on what happens when they win. They don’t notice that that strategy is making them lose more money when they’re losing than they win when they’re winning. The best strategy, of course, minimizes the losses and maximizes the gains. But they don’t think like that; the wins are so seductive that that’s all they pay attention to. Anyway, getting back to the question, these Berkeley epidemiologists invited me to lecture on epidemiology; I said “let me talk about the book”; it gives me a chance to sit down and try to convince some unbiased observers, I hope, that their beliefs about calories-in/calories-out has to be questioned.

INTERVIEWER What effect do you think your lecture had?
TAUBES I don’t know actually. I don’t know how many of the people I was preaching to are already converted. I thought it went over well. I mean, I couldn’t believe that I had spoken for almost two hours and had 90% of the audience awake. There were a few people I lost (you know, you focus on the girl in the seventh row on the right, who’s asleep). But most people seemed pretty attentive. But when I say I’m trying to infect others with these beliefs, if I convinced even a few of the faculty Berkeley that these ideas have to be taken seriously I’ve made progress. OK, now I’ve got a little infection growing at Berkeley. Indeed, I asked one of the epidemiologists who invited me to e-mail, say, ten of his colleagues and say, “You should get Taubes to come lecture, because it’s fascinating, and you might think his book is a little dubious, but when you hear his lecture…”. So we’ll see if it has any effect or if they’ve found it compelling enough that they went through with it. I hope so.

INTERVIEWER I’m just surprised that they found your book dubious. I think they might disagree with your interpretation of the evidence, but I don’t think they would find the reporting dubious.

TAUBES I’ve got to get to the people who take this knee-jerk response that they know what I think, and they don’t have to read the book. For instance, I had lunch with a Berkeley obesity researcher that I’d interviewed five years ago. We spent a couple of hours together five years ago and I sent him a copy of the book when it came out.

INTERVIEWER Who is this?

TAUBES A guy named Marc Hellerstein. He’s a runner and, of course, he believes that sloth is the cause of overweight. He joined us for lunch on Wednesday, but he didn’t eat, and I had about 35 minutes to try and convince him to read the obesity section of the book. The way he sees it, he’s got a lot to do; he’s a busy man, doing all of these experiments, trying to get funding, what could he possibly learn from reading the book and it’s a big book? So I was basically sparring with him for 35 minutes trying to inflict enough damage that he might conclude that he might actually learn something about his own subject of expertise if he reads it. And he actually said “OK, OK, OK, I’m going to read it, I’m going to read it”. (If he does, I’d be surprised, because after the lecture I e-mailed him a few follow-up notes, and he never bothered to respond.) I believe his initial response is probably common among obesity researchers, and even if they’re tempted, they first have to wade through 200 pages on chronic disease that try to convince them that everything else they believed is wrong. The exceptions are those people like you, who already had reason to agree with me.

INTERVIEWER Well, I think your book is a great book, and I don’t think its effect is limited to how many reviews it gets. What books do you think your book resembles? I think of it as a book showing that authorities can be seriously wrong, but what do you think?

TAUBES You know, I don’t know, actually. I can’t answer that question without sounding like a crazed egomaniac, so I won’t. What the book does is try to explain why the paradigm of obesity and chronic disease has to change and then to offer the alternative paradigm. Although I don’t use the word “paradigm” in the second half of the book, that’s what it’s trying to do. I want people to stop thinking about obesity as a disorder of overeating, calories in over calories out, and think about it as a disorder of excess fat accumulation. That’s a classic paradigm shift, or at least so I think. I don’t believe that you can understand obesity and its associated chronic diseases, without thinking of obesity fundamentally as a disorder of excess fat accumulation and asking this question: what regulates fat accumulation? That’s going to be the thing that tells you what the cause of obesity is. If it’s a paradigm shift, then you have to ask yourself how many paradigm shifts are there like this, and what kind of books have been written to directly shift those paradigms, and then I sound like I have some serious ego problems.

INTERVIEWER Then let me put the question differently. I think your book piles up an enormous amount of evidence that is hard to refute. The cumulative effect of all that evidence is not that we’ve been lied to, of course, but that we’ve been misled, badly misled, about something that’s really important, namely our health. So, are there other books like this?

TAUBES I really can’t answer that question either. I’m not erudite enough and then I spent the last five years doing nothing but reading about fats and carbohydrates, so my memory of other subjects fades away. Here’s how I think of it, though: when I was talking with my editor about this book when we in the editing process — and he’s a tremendous editor, who has edited maybe eight or nine non-fiction Pulitzers — I brought up a book called Ashes to Ashes as an example. Ashes to Ashes is by Richard Kluger and it won the Pulitzer and my editor edited it. It’s about the cigarette industry and not just the industry itself, but the science and the struggle to understand that cigarettes cause lung cancer. I said to my editor, “Imagine if we lived in a world where the public health authorities were telling us that lung cancer is caused by saturated fat”. Kluger has got to write a different book, and that’s the situation that we are in.

INTERVIEWER Kluger has got to write a longer book? Was that your argument?

TAUBES He’s got to write a different book. His book was actually longer than mine, but it was a narrative, which mine isn’t. If you’re going to convince the entire public health community that they’ve made a horrible mistake — or many of them, in this case, whether about cigarettes or obesity and disease — then you have to build an argument as carefully and as rigorously as you can. It’s like arguing a legal case, more so than telling a story. And that’s one of the reasons why my book can be difficult to read, or challenging.

INTERVIEWER I found it easy to read.

TAUBES Well, good. See, I read the Amazon reviews. I shouldn’t but I do. And for every three people who say it’s tremendous, there’s somebody who says “It’s boring” and they couldn’t get through 20 pages of it. One problem is that we gave it this diet-like spin, with the title “Good Calories, Bad Calories” and people buy it expecting a diet book. And it’s not a diet book. I also have a lot of friends who tell me they bought the book and they’re jumping into it, and I never hear from them about it. It tells me, being a cynic, that they got to the section on VLDL and LDL or some such, and that was the end of that.

INTERVIEWER I think it has a lot of evidence. I think the book is harder to read than it might be, because you feel compelled to have a lot more evidence than usual, because you’re saying something that everyone says is false. If what you’re saying was more conventional or acceptable or went down more easily, you wouldn’t need as much evidence.

TAUBES Well, that’s the thing. This is one of the ironies, again, of reviews like Gina Kolata’s or some other that I’ve got. They’ll say the book’s too long, it goes on and on, and then they’ll say “he doesn’t even mention X,” or “he leaves out this evidence”. I’m all too aware of the arguments I left out, the counter-arguments, the counter-counter-arguments, the counter-counter-counter-arguments. At one point I had a draft of the book that was 400,000 words, unfinished. For every section, like the section on salt and blood pressure, I would say “here’s why we believe what we’ve come to believe. Here’s the counter-evidence implicating carbohydrates. Here’s how the authority figures treat that counter-evidence. Here’s why they can look at that evidence and think it’s not a challenge to their beliefs”. And my editor, bless his heart, said “Look, you don’t need this. If you get a chance to lecture on this material, then you can tell the people in the audience why their counter-counter-arguments aren’t actually refutations of the carbohydrate hypothesis. You don’t need fifteen different levels in the book.” But, you’re right, I’m trying to convince people of something they don’t believe. I was walking this tightrope between making it readable for the lay public, so that they could make their own decisions, and hoping that doctors, researchers, and authorities would read it, and they might say, “Well, you know, Taubes has a point. Maybe we should take this seriously.” What I fear is that on one level, I lose some of the lay public, because it’s too difficult and advanced, and on the other level, the physicians and researchers aren’t going to read it anyway, because they don’t see that a journalist can tell them anything they don’t already know. And then there’s this effect where, after I challenge half a dozen of their most fundamental beliefs, and they’re only 150 pages into it, do they just burn out? The example that I use there is that if somebody came out with a really-well-reviewed book saying that extrasensory perception should be taken seriously as a scientific phenomenon, I wouldn’t be able to read it. No matter how good it was, or other people thought it was, I wouldn’t be able to read it. I might try, because I tell myself I have to be intellectually honest and rigorous, but I could imagine, after 50 pages, I’d just say “I can’t do it. Maybe he’s right, but I can’t process it. My brain won’t allow me to process what he’s saying”. I wonder if that’s going on here, too: “Saturated fat, OK, but salt, fiber? Give us a break.”

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INTERVIEWER I was impressed with the discussion in your book and lecture about obesity coexisting with poverty in all these different cultures and the implications of that. I’d never seen that before.

TAUBES I have this feeling, and I guess that all writers (or all neurotic writers) have to some extent, that my work is being ignored. It’s my Rodney Dangerfield complex. Now that I’ve written the book, I occasionally get emails from friends saying that they had some discussion with some obesity researcher, and they said, “Are you going to read Taubes’s book?” and their response was “Well, we know what Taubes thinks, so why should I bother reading the book?” What’s more, the Atkins craze has come and gone, so these people believe it’s old news. Why should they pay attention to the book or what I might have learned in reporting it? In fact, I got more reviews for my cold fusion book than I have for Good Calories, Bad Calories. And The cold fusion book came out three years after the fact. There was also this sense that my article started an Atkins craze, and then Atkins Nutritionals declared bankruptcy, and somehow it all went away, and it’s just the same old diet crap that nobody wants to hear about. Nobody is going to stay on the Atkins diet so who cares? Let’s move on. The lecture you heard is an attempt to combat that attitude: I argue that the existence of these obese, impoverished populations living on high carbohydrate diets are counter-examples to the conventional wisdom. As I said in my talk, if you have an obese mother and a malnourished child living in the same family, and this is a common phenomenon, that should be perceived as a refutation of the calories in/calories out hypothesis. In any sort of healthy scientific endeavor, that’s the kind of paradox you look for. Physicists have recently spent a few billion dollars building an accelerator that will, they hope, produce some kind of phenomenon that they can’t explain by their current theory. If they get that, it’s front page news and they now have some observation that they can use to improve their theory. These obesity researchers, they have malnutrition and obesity coexisting in the same impoverished population, and they don’t see it as a challenge to their hypothesis. How do I get the word out that there are important issues here that have to be discussed? That’s what that lecture is intended to do. When [the New York Times reporter] Gina Kolata reviewed my book in the New York Times Book Review, she swept right over these issues. She went right to the thing that bugged her — why don’t people stay on these low-carb diets? — and ignored all the evidence that refutes the conventional wisdom about why we get fat. All she cared about in the end was why don’t people stay on these diets if they work.

INTERVIEWER As if that’s your fault! I thought that was a very unusual way to review a book.

TAUBES Well, she had written her own obesity book that came out five months earlier, and she blamed obesity, in effect, on genes, without bothering to acknowledge that the genes interact with the environment; we have an obesity epidemic; we have obesity associating with poverty, for instance, so there’s obviously some lifestyle factor.

INTERVIEWER And obesity’s gone way up in the recent past; it can’t be genes.

TAUBES I felt her review was her way of saying “Look, this is why none of the stuff he discusses was in my book.” One point I make over and over again is that obesity is a disorder of excess fat accumulation, so you have to look at the hormonal regulation of fat tissue. If you’re discussing growth disorders — gigantism or dwarfism — you look at the hormonal regulation of growth. So why not do the same in obesity. Gina didn’t, because nobody she interviewed brought it up. Then she turned her review of my book into an excuse for why she didn’t mention any of these things. Anyway, that’s life in the publishing industry. If you think about it too much, you just get angry.

Interview directory.

Many studies have linked dairy consumption with an increased risk of prostate cancer. Two studies in a recent issue of the American Journal of Epidemiology looked at this connection in detail and reached the same surprising conclusion: it’s low-fat dairy that is problematic. Here are their abstracts:

High intakes of calcium and dairy products have been suggested to be related to prostate cancer risk. Such associations were examined in the Multiethnic Cohort Study (1993–2002) among 82,483 men who completed a detailed quantitative food frequency questionnaire. During a mean follow-up of 8 years, 4,404 total cases of prostate cancer were identified. In Cox proportional hazards models, no association was found between calcium and vitamin D intake and total, advanced, or high-grade prostate cancer risk, whether for total intake, intake from foods, or intake from supplements, among all male participants or among nonusers of supplemental calcium. No association of calcium or vitamin D intake was seen across racial/ethnic groups. In analyses of food groups, dairy product and total milk consumption were not associated with prostate cancer risk. However, low-/nonfat milk was related to an increased risk and whole milk to a decreased risk of total prostate cancer; after stratification, these effects were limited to localized or low-grade tumors. Although the findings from this study do not support an association between the intakes of calcium and vitamin D and prostate cancer risk, they do suggest that an association with milk consumption may vary by fat content, particularly for early forms of this cancer.

Calcium and dairy foods in relation to prostate cancer were examined in the National Institutes of Health (NIH)-AARP (formerly known as the American Association of Retired Persons) Diet and Health Study (1995/1996–2001). Diet was assessed with a food frequency questionnaire at baseline. Multivariate relative risks and 95% confidence intervals were estimated by Cox regression. During up to 6 years of follow-up (n = 293,888), the authors identified 10,180 total prostate cancer cases (8,754 nonadvanced, 1,426 advanced, and 178 fatal cases). Total and supplemental calcium were unrelated to total and nonadvanced prostate cancer. However, a statistically nonsignificant positive association with total calcium was observed for advanced (≥2,000 vs. 500–<750 mg/day: relative risk (RR) = 1.25, 95% confidence interval (CI): 0.91, 1.71; ptrend = 0.06) and fatal (≥1,000 vs. 500–<750 mg/day: RR = 1.39, 95% CI: 0.92, 2.09; ptrend = 0.10) prostate cancer. Skim milk, but not other dairy foods, was associated with increased risk of advanced prostate cancer (≥2 vs. zero servings/day: RR = 1.23, 95% CI: 0.99, 1.54; ptrend = 0.01). In contrast, calcium from nondairy foods was associated with lower risk of nonadvanced prostate cancer (≥600 vs. <250 mg/day: RR = 0.82, 95% CI: 0.68, 0.99; ptrend = 0.04). Although the authors cannot definitively rule out a weak association for aggressive prostate cancer, their findings do not provide strong support for the hypothesis that calcium and dairy foods increase prostate cancer risk.

Emphasis added. The differences between these two abstracts should interest people trying to learn how to write abstracts.

First article. Second article.

INTERVIEWER You wrote that New York Times piece, and from my take on it, you had a bunch of evidence, and then you got a book contract. Is it fair to say that you found out that what you wrote in the piece was mostly right?

TAUBES It’s a difficult question. I had actually pitched the New York Times piece on fat as an attempt to determine the cause of the obesity epidemic. The proposal was very open ended. I had several ideas. I actually believed, going in to the story, that the answer was going to be that high-fructose corn syrup was responsible for Americans getting fatter over the last 30 years.

INTERVIEWER I’m glad to hear that.

TAUBES The thing about the obesity epidemic is that we can say when it starts, give or take five years: sometime between the mid-1970s and late 1980s. So we have a starting point, and that happens to coincide with the introduction of a type of high-fructose corn syrup known as HFCS-55, which was developed to taste exactly like sugar when it’s put in sodas and juices. In fact, it is effectively identical to sugar, as far as the body is concerned — sugar (sucrose) is 50-50 glucose and fructose and HFCS-55 is 45 percent glucose and 55 percent fructose — although I didn’t know that when I pitched the article. But I thought that high-fructose corn syrup is so cheap. Basically this is an idea that Greg Critser in a book called Fatland picked up on, and subsequently Michael Pollan, too, that high fructose corn syrup allows you to saturate the market with sugar, without any fear that price fluctuations will cause you to go out of business, or lose you a lot of money. If the international price of sugar suddenly spikes, as it did in the 70s, and you’re committed to fulfilling this enormous demand for sugar you’ve created, then you’re in trouble. But if you have a cheap reliable source of sugar, at a price that won’t change from year to year, then you can create an enormous market without fear. This was, more or less, my naive idea of how the economics of HFCS might have caused an entire nation to get fat. Once they had this dependable low-cost sugar substitute, the sugar industry and the soda industry could then expand their production and sell Big Gulps, etc. Then I did the reporting. I talked with industry analysts, and they said that was nonsense; that the primary cost of selling sodas and fruit juices is the bottling and the shipping, and that the cost of the sweeteners is such a tiny portion of the cost of the end product that it wouldn’t have made any difference whether it was sugar or high-fructose corn syrup. So I moved to my next idea, which was based on the fact that the beginning of the obesity epidemic coincided with the institutionalization of the low-fat dogma. As I’m doing that reporting, I stumbled upon what was, at that time, five trials of the Atkins diet, all of which had been finished, but not yet published. At one point, when I was doing the reporting, I actually got worried that some other journalist would beat me to the punch.

INTERVIEWER What was it about the Atkins diet that made these trials so important to your article?

TAUBES: Well, remember, my background, as a journalist and in school, was more or less in physics. In the kind of physics I used to write about, you’ve got some complicated detector that’s looking at particles and atoms smashing together inside it and you’re looking for some byproduct of a collision that you’ve never seen before. A new particle. But the first thing you have to do is make sure you understand your detector. Can you believe what it’s telling you. So you to have to calibrate it. If you want to know how much you weigh, for instance, one thing you might do before you step on the scale is you calibrate that. You make sure that when you’re not on it, the little arrow on the scale is pointing to zero. If it’s registering one or two pounds when you’re not standing on it, then it might be off by five or ten pounds or more when you are. So you want to calibrate your equipment. You want to know that when you set it to zero, it says zero. That’s an idea that’s always resonated with me. Measure what happens at an extreme, make sure you understand that, and then see what happens from there. So here’s the Atkins diet: in theory, you’re removing virtually all of the carbohydrates, but you don’t tell people to eat less. You tell them to eat as much as they want. It’s like you’re setting the diet to zero carbohydrates, and as much fat as possible. According to conventional wisdom, you should certainly not lose weight and you might even gain it. But here were five studies saying that, lo and behold, people really do lose weight when you remove the carbohydrates from the diet, and they lose more weight than they do when you tell them to keep the carbohydrates but eat less calories. What’s more, their cholesterol profiles actually improve, so how can fat or saturated fat be bad for your cholesterol, if these high fat, high saturated fat diets make your cholesterol levels better. To me that had to tell you something about the validity of the low-fat dogma and about the underlying physiology. What do carbohydates do, and what does their removal do. So once I learned about those five studies, I was confident that I had a story that was now worth writing. As for your original question, about whether I found out most of what I originally wrote was right, obviously the book supports the message of the article, but I no longer believe a fair number of things I believed when I wrote that story. For instance, when I wrote the Times article I inherently believed that the key was still calories consumed.

INTERVIEWER You mean things that you believed then, that you don’t believe now?

TAUBES Yes, that I don’t believe now. In that original article, I discussed what David Ludwig has argued — that easily digestible carbohydrates cause these blood sugar and insulin spikes, and that in turn causes blood sugar to plummet, and the result is blood sugar so low a few hours later that this in turn makes you hungry. So you eat more and that’s why you get fat with carb-rich diets. Ludwig works with obese children at Harvard and I believed that his hypothesis was probably true. Then I also talked about Michael Schwartz’s research at the University of Washington. Schwartz believes that insulin’s primary role is to suppress hunger in the brain, but that somehow we become resistant to that effect and so, once again, we eat too much and that’s why we get fat. Both these theories are predicated on the notion that we get fat because we eat too much and that’s what I believed. We consume more calories than we expend and we get fat; something about carbohydrates facilitates that excess consumption. Now I believe the causality is reversed, and that’s what I discuss in the book and in the lecture. Carbohydrates make us accumulate calories in our fat tissue, and that in turn makes us eat too much. It’s all about the regulation of fat metabolism. All those things that Ludwig and Schwartz were talking about might have been true (I mean, they are true, on some level), but they’re not the driving force of why we get fat, or why removing the carbohydrates makes us lean.

INTERVIEWER I see. So that’s a good summing up of what was in your article that you believe, and what you don’t believe anymore.

TAUBES There are other related facts, as well. I never imagined when I wrote that original article that I would come to believe that exercise won’t make you lose weight, even though I’ve been an athlete my entire life and it’s never helped me. So it’s fair to say that when I wrote that New York Times article five years ago, I had an entirely different conception about the causes and cures of obesity and overweight. Carbohydrates were key, but my understanding of the mechanisms was completely different. That’s the kicker with research and reporting: you don’t know what you’ll find until you do it.

Interview directory.

I interviewed Gary Taubes shortly after he gave a talk about the main ideas of his new book — Good Calories, Bad Calories – at UC Berkeley. The interview lasted 2 hours.

INTERVIEWER I just spoke to someone who reduced the carbohydrate in his diet, for various reasons, including your book. He found that his performance on mental problems started improving again. It had stopped improving; it had been constant for a long time, and then it started getting better. So it may be that when you reduce the carbohydrate in your diet, your brain starts working better.

TAUBES Well, there is evidence that your brain works more efficiently on ketones, as does your heart. So if he reduced his carbohydrate consumption sufficiently, he probably increased the level of ketones in his blood. But I’m just speculating here.

INTERVIEWER: The book seems to have had an unusual beginning. You’d been writing about salt, and you learned that a scientist you didn’t trust about salt was also talking about obesity?

TAUBES Well, I’ve spent over 20 years now writing about controversial science. In the mid-1980s, I lived at CERN for ten months, the big physics lab outside Geneva, watching physicists discover non-existent elementary particles. Then I wrote a somewhat infamous story about prions, the supposed causative agents of Mad Cow Disease. I wrote a book about cold fusion: I got obsessed with this question of how it happened, because it was so obviously wrong. After all that, I developed what I believe is a very good feel for who’s a good scientist, and who’s a bad scientist, just by talking to them. There are certain ways that good scientists describe their data, describe the caveats, and describe the conditions by which they may or may not be right. I had also, obviously, with cold fusion, interviewed some of the worst scientists in the world. I used to joke with my friends in the physics community that if you want to cleanse your discipline of the worst scientists in it, every three or four years, you should have someone publish a bogus paper claiming to make some remarkable new discovery — infinite free energy or ESP, or something suitably cosmic like that. Then you have it published in a legitimate journal ; it shows up on the front page of the New York Times, and within two months, every bad scientist in the field will be working on it. Then you just take the ones who publish papers claiming to replicate the effect, and you throw them out of the field. A way of cleaning out the bottom of the barrel.

INTERVIEWER I thought your NY Times article, “What if It’s All Been a Big Fat Lie,” sort of did that. The people who came out against it, they were the bad journalists. Just throw them out!

TAUBES Well, how I got onto that: I was doing this story for Science on salt and blood pressure, looking into the controversy about whether salt consumption plays any role at all in raising blood pressure and causing hypertension. One of the prime players in this salt/blood pressure controversy was obviously one of the worst scientists I’d ever met — one of the five worst…you can’t say, in that five, who is the very worst, but they’re all pretty bad. This is a group that includes guys like Stan Pons and Martin Fleischman who claimed to have discovered cold fusion. While I’m on the phone with this guy, interviewing him, he takes credit for getting Americans to eat less fat and fewer eggs. I literally finished the interview, called my editor at Science, and I said “You know, one of the worst scientists I’ve ever interviewed just took credit for getting Americans to eat less fat and fewer eggs, and I don’t know what the story is, but when I’m done with this salt story, I’m going to look into fat, cholesterol, and saturated fat.” I had a great relationship with Science. My editors had faith in me. If I said there was a story there, they’d give me the support I needed to pursue it. A year later, I ended up with that first story in Science, saying that there’s no evidence that reducing the total fat in the diet makes a damned bit of difference in our health. The evidence that saturated fat and monounsaturated fats are players is, at best, marginal. And that led to the N.Y. Times article.

INTERVIEWER What did that scientist say that made you rank him so low?

TAUBES There are all kinds of signs. He told me there was no controversy, when there was obviously a controversy. His side might have been right, but to deny there as a controversy was ludicrous. He talked about the legitimacy of throwing out negative data. You measure salt consumption one way; you don’t see any effect on blood pressure, and so you decide that’s obviously the wrong way to measure it. The implication of everything he told me was that he knew what the answer was before he did his experiments, and then he adjusted his experimental techniques and methodology until he got the answer that he wanted. And he believed this was legitimate science. There are other signs. I’m a stickler about the use of words like “evidence” and “proof”. So if someone tells you there’s no evidence for some controversial belief, you can be fairly confident that they’re a bad scientist. There’s always evidence, or there wouldn’t be a controversy. If somebody says that “we proved that this was true” or “we set out to prove that this was true” that’s another bad sign. The point here, as Popper noted, among others, is that you can never prove anything is true; you can only refute it. So researchers who talk about proving a hypothesis is true rather than testing it make me worried.

INTERVIEWER Yeah, I see what you’re saying. They overstate; they twist things around to make it come out the way they want. They are way too sure of what they…

TAUBES Yes, and the really good scientists are the ones, almost by definition, who are most skeptical of evidence that seems to support their beliefs. They’re most aware of how they could have been fooled, how they could have screwed up, or how they might have missed artifacts in their experiment that could have explained what they observed. They’re very careful about what they say. If you ask them to do play devil’s advocate, and tell you how they could have screwed up, then at the very least, they’ll say “Well, if I knew how I could have done it, I would have checked it before I made the claim”. So when I’m talking about discerning the difference between a good scientist and a bad scientist, I’m talking about how they speak about their research, the evidence itself, it’s presence or absence. My friends in journalism would often ask me this question: by what right do I think make decisions about who’s a good scientist and who’s not. I’d say “Well, when you’re an English major, you can be confident that Norman Mailer was a better writer than John Grisham, even though John Grisham makes 10 to 100 times more money”. It’s just a feel for what you do; I don’t know how else to describe it. I know a good scientist when I talk with one. I might be fooled, on occasion, but….

INTERVIEWER It’s not particularly well-correlated with how famous they are, or how many Nobel Prizes they’ve won.

TAUBES My first book was about a Nobel Prize winner who discovered non-existent elementary particles.

INTERVIEWER Who was that?

TAUBES An Italian physicist named Carlo Rubbia.